| First Author | Li G | Year | 2017 |
| Journal | Cell Death Dis | Volume | 8 |
| Issue | 5 | Pages | e2811 |
| PubMed ID | 28542142 | Mgi Jnum | J:301834 |
| Mgi Id | MGI:6507299 | Doi | 10.1038/cddis.2017.124 |
| Citation | Li G, et al. (2017) Deletion of Pdcd5 in mice led to the deficiency of placenta development and embryonic lethality. Cell Death Dis 8(5):e2811 |
| abstractText | Programmed cell death 5 (PDCD5) is an apoptosis promoter molecule that displays multiple biological activities. However, the function of PDCD5 in vivo has not yet been investigated. Here, we generated a Pdcd5 knockout mouse model to study the physiological role of PDCD5 in vivo. Knockout of the Pdcd5 gene resulted in embryonic lethality at mid-gestation. Histopathological analysis revealed dysplasia in both the LZs and JZs in Pdcd5(-/-) placentas with defects in spongiotrophoblasts and trophoblast giant cells. Furthermore, Pdcd5(-/-) embryos had impaired transplacental passage capacity. We also found that Pdcd5(-/-) embryos exhibited cardiac abnormalities and defective liver development. The growth defect is linked to impaired placental development and may be caused by insufficient oxygen and nutrient transfer across the placenta. These findings were verified in vitro in Pdcd5 knockout mouse embryonic fibroblasts, which showed increased apoptosis and G0/G1 phase cell cycle arrest. Pdcd5 knockout decreased the Vegf and hepatocyte growth factor (Hgf) levels, downregulated the downstream Pik3ca-Akt-Mtor signal pathway and decreased cell survival. Collectively, our studies demonstrated that Pdcd5 knockout in mouse embryos results in placental defects and embryonic lethality. |
